树突状细胞和动脉粥样硬化

树突状细胞是最有效的抗原递呈细胞。自1995年于动脉中发现树突状细胞以来，对于其在动脉粥样硬化形成中的重要性有了进一步的认识。在动脉粥样硬化的很早期血管树突状细胞就被激活。部分细胞直接与T细胞聚集成簇在动脉粥样硬化病变中，其他则移行至淋巴器官激活T细胞。内皮功能改变和血脂紊乱影响树突状细胞的功能，最近研究发现树突状细胞在斑块不稳定中起重要作用。本文综述树突状细胞与动脉粥样硬化的关系。     

树突状细胞在动脉粥样硬化中的作用

基础和临床研究均证实,炎症反应在动脉粥样硬化(atherosclerosis,AS)的发生、发展及其导致的临床事件过程中起着重要作用.在发生AS的血管内膜和粥样斑块中可见T淋巴细胞、巨噬细胞以及树突状细胞(dendritic cell,DC)聚集现象.作为激活T淋巴细胞最主要的抗原提呈细胞,DC具有决定T淋巴细胞活化、凋亡以及聚集等的重要功能.文章就DC与AS病变的相关性进行了综述.     

树突状细胞与动脉粥样硬化

树突状细胞 (dendriticcell)是一种广泛分布于机体各组织的抗原递呈细胞。最近人们发现 ,树突状细胞也存在于动脉壁中 ,并且在动脉粥样硬化 (atherosclerosis ,AS)斑块中聚集增多 ;它们与T细胞等免疫活性细胞之间存在直接的接触联系 ,并表达共刺激分子CD4 0和热休克蛋白 (heatshockprotein ,HSP)等。提示树突状细胞在AS的发生、发展中起着重要作用。我们就血管壁中的树突状细胞及其在AS发生、发展中的作用作一综述 ,并对其在治疗AS方面的前景作一展望。　　一、正常动脉壁内存在树突状细胞　　 1995年 ,Bobryshev和Lord〔1〕 在没有A…     

树突状细胞和动脉粥样硬化

动脉粥样硬化与炎症免疫密切相关.树突状细胞是目前发现的体内功能最强大的专职抗原呈递细胞,参与体内许多自身免疫性疾病的发生.近来的研究发现树突状细胞可能在动脉粥样硬化形成中起着重要的作用.本文就现有的关于树突状细胞的生物学特性及其在动脉粥样硬化形成中所扮演的角色和未来的可能治疗应用作一综述.     

树突状细胞在动脉粥样硬化发生发展中的作用

动脉粥样硬化是一种通过内皮细胞触发和持久炎症的慢性疾病。最近研究显示树突状细胞在动脉粥样硬化形成过程中起重要的作用。树突状细胞是与动脉粥样硬化发生发展有关的有效抗原递呈细胞和免疫调节细胞。氧化型低密度脂蛋白、缺氧、尼古丁和热休克蛋白等可导致内皮功能失调,从而影响树突状细胞的黏附和成熟。大量证据证明炎性/免疫活性斑块是导致急性冠状综合征的主要原因之一。在动脉粥样硬化斑块中含有大量的树突状细胞和T淋巴细胞。他汀类药物和地尔硫卓能抑制树突状细胞刺激T细胞反应,从而防止动脉粥样硬化的发生发展。     

树突状细胞与自身免疫性甲状腺疾病

树突状细胞是一类专职抗原提呈细胞，在自身免疫性甲状腺疾病中，甲 状腺细胞的异常生长和代谢，细胞因子和粘附分子等因素都可能趋使其在甲状腺内的聚集，树突状细胞通过提呈抗原，激活T细胞，分泌细胞因子等功能在启动和维持自身免疫性甲状腺疾病中起重要作用，还可对甲状腺细胞生长和激素分泌产生影响。     

树突状细胞与自身免疫性甲状腺疾病

树突状细胞是一类专职抗原提呈细胞 ,在自身免疫性甲状腺疾病中 ,甲状腺细胞的异常生长和代谢、细胞因子和粘附分子等因素都可能趋使其在甲状腺内的聚集。树突状细胞通过提呈抗原、激活T细胞、分泌细胞因子等功能在启动和维持自身免疫性甲状腺疾病中起重要作用 ,还可对甲状腺细胞生长和激素分泌产生影响。     

树突状细胞和动脉粥样硬化

动脉粥样硬化与炎症免疫密切相关。树突状细胞是目前发现的体内功能最强大的专职抗原呈递细胞，参与体内许多自身免疫性疾病的发生。近来的研究发现树突状细胞可能在动脉粥样硬化形成中起着重要的作用。本文就现有的关于树突状细胞的生物学特性及其在动脉粥样硬化形成中所扮演的角色和未来的可能治疗应用作一综述。     

树突状细胞在血吸虫感染中的作用

树突状细胞（DC）是一类重要的专职抗原提呈细胞（APC）,广泛分布于除脑外的全身各个组织器官,但数量极少,血吸虫感染机体后,不成熟的DC识别血吸虫抗原并成熟,再由外周组织通过淋巴管或血液循环迁徙至次级淋巴器官,刺激T细胞增殖,发生免疫应答。本文就树突状细胞在血吸虫感染中的免疫保护作用以及参与血吸虫的免疫逃逸中的作用机制作简要概述。     

树突状细胞在老化中的作用

树突状细胞目前普遍被认为是最强有力的抗原提呈细胞，对体内静息T细胞的激活最有效率，因此，作为免疫系统的始动者，它们正在成为免疫学研究的核心，并被认为是免疫疗法中很有用的工具。它们也可能弥补缺陷T细胞的反应能力。除去树突状细胞在分子和细胞生物学的许多最新进展外，仅有少数文献提及树突状细胞与老化的课题。     

Role of dendritic cells in atherosclerosis

Atherosclerosis is a lipid-related chronic inflammatory disease in which immune mechanisms play a pivotal role. The lesions are filled with large numbers of immune cells. During the last decade, dendritic cells have been identified in atherosclerotic plaques and are thought to play an important role in atherogenesis. Dendritic cells express major histocompatibility complex I and II, human leukocyte antigen-DR, CD1a, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and co-stimulatory molecule on their surfaces and this explains their unique ability to activate naive T cells. Factors such as oxidized low-density lipoprotein, hypoxia, nicotine, heat shock proteins, and altered nitric oxide synthase activity of the endothelium, all of which cause endothelial dysfunction, have a significant impact on dendritic cell adherence to endothelium and maturation. Mature dendritic cells are capable of presenting antigens to T cells, and activation of T cells leads to release of cytokines, which play an important role in the progression of disease. Drugs such as statins and diltiazem have been shown to protect endothelial function by inhibition of dendritic cell-endothelial cell interaction, and can be applied to delay the progression of cardiovascular diseases.     

Replication of human immunodeficiency virus type 1 in primary dendritic cell cultures.

The ability of the human immunodeficiency virus type 1 (HIV-1) to replicate in primary blood dendritic cells was investigated. Dendritic cells compose less than 1% of the circulating leukocytes and are nondividing cells. Highly purified preparations of dendritic cells were obtained using recent advances in cell fractionation. The results of these experiments show that dendritic cells, in contrast to monocytes and T cells, support the active replication of all strains of HIV-1 tested, including T-cell tropic and monocyte/macrophage tropic isolates. The dendritic cell cultures supported much more virus production than did cultures of primary unseparated T cells, CD4+ T cells, and adherent as well as nonadherent monocytes. Replication of HIV-1 in dendritic cells produces no noticeable cytopathic effect nor does it decrease total cell number. The ability of the nonreplicating dendritic cells to support high levels of replication of HIV-1 suggests that this antigen-presenting cell population, which is also capable of supporting clonal T-cell growth, may play a central role in HIV pathogenesis, serving as a source of continued infection of CD4+ T cells and as a reservoir of virus infection.     

Characterization of colonic and mesenteric lymph node dendritic cell subpopulations in a murine adoptive transfer model of inflammatory bowel disease

Ulcerative colitis and Crohn's disease, collectively termed inflammatory bowel diseases (IBD), are chronic inflammatory diseases of the intestine that afflict more than 4 million people worldwide. Intestinal inflammation is characterized by an abnormal mucosal immune response to normally harmless antigens in the gut flora. In Crohn's disease, the pathogenic mucosal immune response is a typical T helper (TH1) type cell response, whereas ulcerative colitis is predominantly associated with a TH2 response. We are interested in the role of dendritic cells in early immunologic events leading to T cell activation and chronic intestinal inflammation. Using a murine adoptive transfer model of IBD, we found an accumulation of dendritic cells in colon and mesenteric lymph nodes during the early stage of IBD before the appearance of epithelial lesions and tissue degradation. In situ immunostaining and flow-cytometric analysis revealed that approximately 50% of colonic dendritic cells were CD11b B220 myeloid dendritic cells and 50% expressed the CD11b B220 plasmacytoid phenotype. In corresponding mesenteric lymph nodes, approximately 16% were plasmacytoid dendritic cells. Colonic myeloid dendritic cells were shown to express the co-stimulatory molecule CD40. Both, colonic myeloid and plasmacytoid dendritic cells released interferon-alpha in situ and stimulated T cell proliferation ex vivo. Our results show that dendritic cells can mature in the intestine without migrating to mesenteric lymph nodes. Mature intestinal dendritic cells may form a nucleation site for a local T cell response and play an important role in the pathogenesis of IBD.     

Platelet activation responses in vitro to human mast cell activation

Mast cells are thought to play an important role in atherogenesis and plaque rupture, but their role in the subsequent platelet activation and thrombus formation is unclear. Tryptase positive cells (KU812T+) were established from the KU812 cell line as an in vitro model of human mast cells and used to study the effect of mast cell activation on human platelets. Overnight incubation of KU812T+ with IgE and subsequent challenge with anti-IgE caused the release of heparinoid substances which inhibited 1 microg/ml collagen-induced platelet aggregation. KU812T+ challenged with compound 48/80 produced a releasate that had no apparent heparinoid content but caused full platelet aggregation. These findings showed that, although activation of KU812T+ via FcepsilonR1 partially abrogated collagen-induced platelet aggregation, activation of the C5a receptor signalling pathway, by compound 48/80, caused the release of potent platelet-activating substances. This cell culture model offers a unique insight into the role of platelet-mast cell interactions in arterial thrombogenesis.     

Enhancement of dendritic cell activation via CD40 ligand-expressing γδ T cells is responsible for protective immunity to Plasmodium parasites

Previous reports have shown that γδ T cells are important for the elimination of malaria parasites in humans and mice. However, how γδ T cells are involved in protective immunity against blood-stage malaria remains unknown. We infected γδ T-cell-deficient (TCRδ-KO) mice and control wild-type mice with Plasmodium berghei XAT, which is a nonlethal strain. Although infected red blood cells were eliminated within 30 d after infection, TCRδ-KO mice could not clear the infected red blood cells, showed high parasitemia, and eventually died. Therefore, γδ T cells are essential for clearance of the parasites. Here, we found that γδ T cells play a key role in dendritic cell activation after Plasmodium infection. On day 5 postinfection, γδ T cells produced IFN-γ and expressed CD40 ligand during dendritic cell activation. These results suggest that γδ T cells enhance dendritic cell activation via IFN-γ and CD40 ligand-CD40 signaling. This hypothesis is supported strongly by the fact that in vivo induction of CD40 signaling prevented the death of TCRδ-KO mice after infection with P. berghei XAT. This study improves our understanding of protective immunity against malaria and provides insights into γδ T-cell-mediated protective immunity against various infectious diseases.     

树突状细胞与慢性阻塞性肺疾病

慢性阻塞性肺疾病（COPD）是一种慢性炎症性疾病,其病灶局部存在中性粒细胞、巨噬细胞和T淋巴细胞（尤其是CD8^＋T细胞）浸润。吸烟是COPD发病的首要诱因,目前已证实T细胞对于吸烟所致COPD的发生发展具有重要作用;树突状细胞（DCs）是已知的功能最强的抗原提呈细胞,可激活初始T细胞,在诱导和调节免疫应答中发挥关键作用。近年来发现DCs也存在于COPD病灶中,且其功能和数量均发生了改变,提示其可能与吸烟所致COPD的发病机制有关。     

Cardiac dendritic cells and acute myocarditis in the human heart

Cardiac dendritic cells are considered to play an important role in the immunoresponse of the heart. However, it is unclear whether these cells occur in human myocarditis and whether they function in similar ways to those in rats. Cardiac samples were obtained from 22 autopsied patients with myocarditis, and compared with 20 age-and sex-matched controls. Formalin-fixed hearts were immunostained by the LSAB method. Cardiac dendritic cells were detectable even in the control hearts (1.5 cells/high power field (HPF)). In the acute phase of myocarditis, the number of cardiac dendritic cells increased up to 12.6 cells/HPF (p<0.001). In the subacute phase of myocarditis, T cells (36.6 cells/HPF) and HLA-DR+ cells (10.2 cells/HPF) continued to infiltrate the periphery of the inflammatory lesions, but they had no expression without inflammation. In this study, cardiac dendritic cells were reactive for HLA-DR, but negative for CD68, and were characteristically large monocytes with long, slender, dendritic processes. Accordingly, they were clearly distinguishable from macrophages. In the human heart, cardiac dendritic cells may be recruited in the acute phase of myocarditis, and seem to play an important role in the succeeding immunoresponse.     

The role of T cells in the development of cardiovascular disease in HIV-infected patients

Cardiovascular disease (CVD) is highly prevalent in HIV-infected patients. Besides the classical cardiovascular risk factors, HIV related factors play a role, such as immune activation and treatment with highly active antiretroviral therapy (HAART). The resulting T cell activation is regarded as one of the driving forces behind this accelerated atherogenesis. Interventions, such as early treatment and anti-inflammatory therapy, decreasing T cell activation might lead to a lower incidence of CVD in future HIV infected patients. This review specifically explores the role of T cells in the development of atherosclerosis in HIV-infected patients.     

CD8+ cytotoxic lymphocytes in cutaneous leishmaniasis

OBJECTIVE: Review of the literature on the role of CD8+ T cell in the immune response against Leishmania species that cause cutaneous leishmaniasis. The role of macrophages, dendritic cells, CD4 T cells and NK cells has been extensively analyzed in leishmaniasis, yet very little knowledge has been gained on CD8+ T cells in this disease. Murine models of leishmaniasis suggest that CD8+ T cells participate through IFNg production, yet their cytotoxic capacity may also play a crucial role, as has been found in human disease. It is an enigma what mechanisms underlie the CD8+ T cell activation. It is possible that dendritic cells activate CD8+ T cells through mechanisms that include antigen traspresentation. A better understanding of CD8+ T cells in the immune response against Leishmania will undoubtedly provide new insights into the physiopathogenesis of the disease that could lead to new therapeutic approaches against leishmaniasis.     

树突状细胞在支气管哮喘中的作用研究进展

支气管哮喘是由多种免疫细胞和炎性细胞因子参与发病的免疫系统性疾病.在支气管哮喘免疫过程发生的初始和维持阶段,树突状细胞对于过敏原的识别,摄取和提呈,CD4+T辅助细胞的分化和活化,以及气道变态反应和机体免疫耐受等方面发挥关键作用.通过干预树突状细胞在支气管哮喘发病机制中的作用,来达到治疗支气管哮喘的目的,已经成为目前指导临床用药的研究热点.